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OCD:Theoretical approaches
*OCD: Biological perspective *OCD: Evolutionary-neurodevelopmental perspective *OCD: Psychodynamic perspective *OCD: Cognitive perspective *OCD: Interpersonal perspective There are many different theories about the cause of obsessive-compulsive disorder. Some research has discovered a type of size abnormality in different brain structures. The majority of researchers believe that there is some type of abnormality in the neurotransmitter serotonin, among other possible psychological or biological abnormalities; however, it is possible that this activity is the brain's response to OCD, and not its cause. Serotonin is thought to have a role in regulating anxiety, though it is also thought to be involved in such processes as sleep and memory function. This neurotransmitter travels from one nerve cell to the next via synapses. In order to send chemical messages, serotonin must bind to the receptor sites located on the neighboring nerve cell. It is hypothesized that OCD sufferers may have blocked or damaged receptor sites that prevent serotonin from functioning to its full potential. This suggestion is supported by the fact that many OCD patients benefit from the use of Selective Serotonin Reuptake Inhibitors (SSRIs)—a class of antidepressant medications that allow for more serotonin to be readily available to other nerve cells. (For more about this class of drugs, see the section about potential treatments for OCD.) (BBC Science and Nature, accessed 4/15/06). Recent research has revealed a possible genetic mutation that could be the cause of OCD. Researchers funded by the National Institutes of Health have found a mutation in the human serotonin transporter gene, hSERT, in unrelated families with OCD. Moreover, in his study of monozygotic twins, Rasmussen (1994) produced data that supported the idea that there is a “heritable factor for neurotic anxiety”. In addition, he noted that environmental factors also play a role in how these anxiety symptoms are expressed. However, various studies on this topic are still being conducted and the presence of a genetic link is not definite as of yet. Technological advancements have allowed for the possibility of brain imaging. Using tools like positron emission tomography (PET scans), it has been shown that those with OCD tend to have brain activity that differs from those who do not have this disorder (Tennen, accessed 4/14/06). This suggests that brain functioning in those with OCD may be impaired in some way. A popular explanation for OCD is that offered in the book 'Brain Lock' by Jeffrey Schwartz, which suggests that OCD is caused by the part of the brain that is responsible for translating complex intentions (e.g., "I will pick up this cup") into fundamental actions (e.g., "move arm forward, rotate hand 15 degrees, etc.") failing to correctly communicate the chemical message that an action has been completed. This is perceived as a feeling of doubt and incompleteness which then leads the individual to attempt to consciously deconstruct their own prior behavior - a process which induces anxiety in most people, even those without OCD. It has been theorized that a miscommunication between the orbital-frontal cortex, the caudate nucleus, and the thalamus may be a factor in the explanation of OCD. The orbital-frontal cortex (OFC) is the first part of the brain to notice whether or not something is amiss. When the OFC notices that something is wrong, it sends an initial “worry signal” to the thalamus. When the thalamus receives this signal, it in turn sends signals back to the OFC to interpret the worrying event. The caudate nucleus lies between the OFC and the thalamus and it prevents the initial worry signal from being sent back to the thalamus after it has already been received. However, it is suggested that in those with OCD, the caudate nucleus does not function properly, and therefore does not prevent this initial signal from recurring. This causes the thalamus to become hyperactive and creates a virtually never-ending loop of worry signals being sent back and forth between the OFC and the thalamus. The OFC responds by increasing anxiety and engaging in compulsive behaviors in an attempt to relieve this apprehension (BBC Science and Nature, accessed 4/15/06).